Course of platelet counts in cirrhotic patients after implantation of a transjugular intrahepatic portosystemic shunt - a prospective, controlled study

Gschwantler, Michael; Vavrík, J; Gebauer, A; Kriwanek, S.; Schrutka-Kölbl, C; Fleischer, Johannes; Madani, Babak; Brownstone, Eva; Tscholakoff, D; Weiß, W.

doi:10.1016/s0168-8278(99)80071-3

Cited by 28 publications

(24 citation statements)

References 23 publications

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“…There is conflicting evidence on the effect of surgical shunts and the less-invasive transjugular intrahepatic portosystemic shunt (TIPS) on hypersplenism in cirrhotic liver (albeit in methodologically flawed analyses), with some groups demonstrating an improvement in platelet counts after shunt procedures [62][63][64][65][66][67][68][69][70] and others showing no effect. 41,[71][72][73][74][75][76] The majority of the studies were retrospective, with no control group.…”

Section: Hypersplenic Thrombocytopeniamentioning

confidence: 99%

Thrombocytopenia in chronic liver disease

Peck‐Radosavljevic

2016

Liver International

226

180

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Thrombocytopenia is a common haematological disorder in patients with chronic liver disease. It is multifactorial and severity of liver disease is the most influential factor. As a result of the increased risk of bleeding, thrombocytopenia may impact upon medical procedures, such as surgery or liver biopsy. The pathophysiology of thrombocytopenia in chronic liver disease has long been associated with the hypothesis of hypersplenism, where portal hypertension causes pooling and sequestration of all corpuscular elements of the blood, predominantly thrombocytes, in the enlarged and congested spleen. Other mechanisms of importance include bone marrow suppression by toxic substances, such as alcohol or viral infection, and immunological removal of platelets from the circulation. However, insufficient platelet recovery after relief of portal hypertension by shunt procedures or minor and transient recovery after splenic artery embolization have caused many to question the importance and relative contribution of this mechanism to thrombocytopenia. The discovery of the cytokine thrombopoietin has led to the elucidation of a central mechanism. Thrombopoietin is predominantly produced by the liver and is reduced when liver cell mass is severely damaged. This leads to reduced thrombopoiesis in the bone marrow and consequently to thrombocytopenia in the peripheral blood of patients with advanced-stage liver disease. Restoration of adequate thrombopoietin production post-liver transplantation leads to prompt restoration of platelet production. A number of new treatments that substitute thrombopoietin activity are available or in development.

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Section: Hypersplenic Thrombocytopeniamentioning

confidence: 99%

Thrombocytopenia in chronic liver disease

Peck‐Radosavljevic

2016

Liver International

226

180

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“…The hypersplenism mechanism in patients with advanced liver disease is secondary to portal hypertension. Nevertheless, in some cirrhotic patients thrombocytopenia may persist even after splenectomy or after portal decompression [13][14][15][16][17]. Since the return to a normal platelet count has been observed following liver transplantation [18], it is likely that other mechanisms apart from hypersplenism, such as reduced thrombopoietin release by the liver [19][20][21][22], autoimmune thrombocytopenia [23,24], antiretroviral therapy [25], or bone marrow suppression [26,27], are involved in the thrombocytopenia of CLD.…”

Section: Introductionmentioning

confidence: 99%

Thrombocytopenia in patients with hepatitis B virus-related chronic hepatitis: Evaluation of the immature platelet fraction

Dou

Lou

et al. 2013

Platelets

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The immature platelet fraction (IPF) measures the number of reticulated platelets in peripheral blood, and can be used to help determine if thrombocytopenia is secondary to low-platelet production or increased platelet turnover. The aim of this study was to determine whether abnormalities in the IPF were associated with thrombocytopenia in patients with hepatitis B virus-related chronic hepatitis (CHB). One hundred fifty-six patients with chronic hepatitis B, including 80 thrombocytopenia, 76 without thrombocytopenia, and 48 healthy controls were enrolled in the study. The IPF percentages (IPF%) were measured using a XE-2100 multiparameter automatic hematology analyzer. We demonstrated that in the thrombocytopenic group, the IPF% was significantly increased compared with that in healthy controls and the non-thrombocytopenic group (both p < 0.001). Multivariate analysis demonstrated that IPF%, splenomegaly, and the model for end-stage liver disease score were independent predictors for thrombocytopenia (both p < 0.001). High IPF% during the course of thrombocytopenia suggests that platelet destruction/sequestration due to hypersplenism is a major factor contributing to thrombocytopenia in patients with CHB.

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“…However, some controversial reports have noted that thrombocytopenia may persist even after splenectomy or partial decompression (Pradella et al 2011; Sanyal et al 1996; Gschwantler et al 1999). …”

Section: Introductionmentioning

confidence: 99%

Long-term dynamics of hematological data and spleen volume in cirrhotic patients after liver transplantation-various dynamics depending on etiology

et al. 2013

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BackgroundHypersplenism is a common complication in cirrhotic patients, and liver transplantation would be one of the effective treatments. However, detailed dynamics, especially over a long term, are not fully understood. We investigated the long-term dynamics of hematological data and spleen volumes, as well as their correlation in cirrhotic patients who underwent liver transplantation.Patients and methodsWe studied 53 cirrhotic patients who underwent liver transplantation at our institute and followed for more than 1 year. Hematological data were collected from medical records, while spleen volumes were determined by CT volumetry at 0, 1, 3, 6, 12, 24, 36, 48, 60 postoperative months (POM).Results(1) Platelet (Plt) and hemoglobin (Hb) levels were gradually increased up to 18 and 10 POM, respectively, in contrast with white blood cells (WBC), which remained mostly unchanged from pretransplantation levels. (2) Spleen volume was sharply decreased in the first POM, then showed a slower but steady decline up to 48 POM. (3) Spleen volume was significantly correlated with hematological data, though the levels were generally weak (Plt: r = 0.433, p < 0.001; Hb: r = 0.233, p < 0.001; WBC: r = 0.217, p = 0.001). (4) Spleen volume was strongly correlated with all hematological parameters in HBV patients (Plt: r = 0.617, p < 0.0001; Hb: r = 0.401, p < 0.001; WBC: r = 0.387, p < 0.001), in contrast with that in other etiologies, which had generally weak correlations though some were statistically significant.ConclusionsWe investigated the long-term dynamics of hematological data and spleen volume in cirrhotic patients after liver transplantation. Unique dynamics and correlations between them were found among the different etiologies investigated.

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Course of platelet counts in cirrhotic patients after implantation of a transjugular intrahepatic portosystemic shunt - a prospective, controlled study

Cited by 28 publications

References 23 publications

Thrombocytopenia in chronic liver disease

Thrombocytopenia in chronic liver disease

Thrombocytopenia in patients with hepatitis B virus-related chronic hepatitis: Evaluation of the immature platelet fraction

Long-term dynamics of hematological data and spleen volume in cirrhotic patients after liver transplantation-various dynamics depending on etiology

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